Linked Life Data

10078531

Source:http://linkedlifedata.com/resource/pubmed/id/10078531

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6722
pubmed:dateCreated
1999-3-25
pubmed:abstractText
Cyclic ADP-ribose (cADPR) is a natural compound that mobilizes calcium ions in several eukaryotic cells. Although it can lead to the release of calcium ions in T lymphocytes, it has not been firmly established as a second messenger in these cells. Here, using high-performance liquid chromatography analysis, we show that stimulation of the T-cell receptor/CD3 (TCR/CD3) complex results in activation of a soluble ADP-ribosyl cyclase and a sustained increase in intracellular levels of cADPR. There is a causal relation between increased cADPR concentrations, sustained calcium signalling and activation of T cells, as shown by inhibition of TCR/CD3-stimulated calcium signalling, cell proliferation and expression of the early- and late-activation markers CD25 and HLA-DR by using cADPR antagonists. The molecular target for cADPR, the type-3 ryanodine receptor/calcium channel, is expressed in T cells. Increased cADPR significantly and specifically stimulates the apparent association of [3H]ryanodine with the type-3 ryanodine receptor, indicating a direct modulatory effect of cADPR on channel opening. Thus we show the presence, causal relation and biological significance of the major constituents of the cADPR/calcium-signalling pathway in human T cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
4
pubmed:volume
398
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
70-3
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Regulation of calcium signalling in T lymphocytes by the second messenger cyclic ADP-ribose.
pubmed:affiliation
Department of Enzyme Chemistry, Institute of Physiological Chemistry, University of Hamburg, Germany. guse@uke.uni-hamburg.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't